High sympathetic tone, also referred to as autonomic imbalance, is a character of many heart diseases, especially in heart failure (HF) and acute myocardial infarction (AMI). β-blockers are the primary medication to counter balance the increased sympathetic activities. The autonomic system controls physiological activities of the body and the imbalance of autonomic tone is related to many diseases and conditions. Vagal stimulation is an electrophysiological approach to counter balance autonomic imbalance.
Neural stimulation has been the subject of a number of studies and has been proposed to treat sleep disorders, gastrointestinal motility, eating disorders, obesity, anorexia, gastrointestinal tract disorders, hypertension, coma, and epilepsy. Electrical stimulation of parasympathetic nerves can elicit the baroreflex, inducing a reduction of sympathetic nerve activity and reducing blood pressure by decreasing vascular resistance. The baroreflex naturally starts from receptors. Vagal afferent fibers, for example, innervate and mediate the baroreflex. Parasympathetic stimulation counteracts sympathetic activity, which further reduces heart rate and blood pressure. In a congestive heart failure (CHF) patient, the patient's sympathetic tone increases and catecholamine increase. Increased sympathetic tone and catecholamine can cause increased cardiac oxygen consumption, cardiac hypertrophy (remodeling), worsening heart failure, and sudden cardiac death. Vagus nerve stimulation may antagonize sympathetic tone, and may prevent sudden cardiac death. The vagal stimulation counteracts the high sympathetic tone associated with CHF, resulting in a decreased heart rate, reduced oxygen demand, increased diastolic period, and reduced incidence of ventricular arrhythmia. A decrease in the sympathetic tone decreases the excitability of the heart, which decreases arrhythmias. Modulation of the sympathetic and parasympathetic nervous system with neural stimulation has been shown to have positive clinical benefits, such as protecting the myocardium from further remodeling and predisposition to fatal arrhythmias following a myocardial infarction.